Quantitative analysis of the effect of Helicobacter pylori on the expressions of SOX2, CDX2, MUC2, MUC5AC, MUC6, TFF1, TFF2, and TFF3 mRNAs in human gastric carcinoma cells.
OBJECTIVE
To investigate the phenotypic characters of carcinoma cells and the response of gastric epithelial cells to Helicobacter pylori (H. pylori) infection using the gastric carcinoma cell lines.


METHODS
Real-time reverse transcription-polymerase chain reaction (RT-PCR) was used to assess the effect of H. pylori infection on mRNA levels of transcription factors (SOX2 and CDX2), mucin core proteins (MUC2, MUC5AC, and MUC6), and trefoil factor family peptides (TFF) (TFF1, TFF2, and TFF3) in gastric carcinoma cells (AGS, MKN45, and KATO III cells). H. pylori ATCC 43504 and its isogenic cag pathogenicity island (PAI) deleted mutant were used.


RESULTS
These cell lines expressed mixed gastric and intestinal phenotypes. The intestinal phenotype predominated in AGS cells and gastric phenotypes in MKN45 and KATO III cells. In all three cell lines, H. pylori infection inhibited SOX2 mRNA expression, but induced the three TFFs mRNAs. In AGS cells, H. pylori induced cag PAI-dependent mRNA expression of CDX2, MUC2, MUC5AC, and MUC6. mRNA expressions of CDX2, MUC5AC, and MUC6 were inhibited in KATO III cells, whereas MUC2 mRNA expression was unchanged. In MKN45 cells, H. pylori induced the three MUCs mRNAs but inhibited CDX2 mRNA expression.


CONCLUSIONS
This study provides a useful platform for selecting appropriate cell lines to model H. pylori-related changes in the gastric epithelium that mirror the changes seen in vivo. The outcome of H. pylori infection may reflect changes in the mucus gel layer caused by altered expression of mucins and TFF peptides.
Matsuda
Kazuyuki
K
Department of Laboratory Medicine, Shinshu University Hospital, Asahi, Matsumoto, Japan.
Yamauchi
Kazuyoshi
K
Matsumoto
Takehisa
T
Sano
Kenji
K
Yamaoka
Yoshio
Y
Ota
Hiroyoshi
H
D000071616:CDX2 Transcription Factor; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000032:analysis; D024002:HMGB Proteins / Q000032:analysis; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori; D018398:Homeodomain Proteins / Q000032:analysis; D006801:Humans; D055271:Mucin 5AC; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins / Q000032:analysis*; D010455:Peptides / Q000032:analysis*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055748:SOXB1 Transcription Factors; D013274:Stomach Neoplasms / Q000378:metabolism*; D014157:Transcription Factors / Q000032:analysis*; D000071163:Trefoil Factor-1; D000071164:Trefoil Factor-2; D000071165:Trefoil Factor-3; D014407:Tumor Cells, Cultured; D025521:Tumor Suppressor Proteins / Q000032:analysis
D000071616:CDX2 Transcription Factor; C491270:CDX2 protein, human; D004268:DNA-Binding Proteins; D024002:HMGB Proteins; D018398:Homeodomain Proteins; C524625:MUC2 protein, human; C524678:MUC5AC protein, human; C524734:MUC6 protein, human; D055271:Mucin 5AC; D055262:Mucin-2; D055272:Mucin-6; D009077:Mucins; D010455:Peptides; D012333:RNA, Messenger; C527782:SOX2 protein, human; D055748:SOXB1 Transcription Factors; C051838:TFF1 protein, human; C000604007:TFF2 protein, human; C082495:TFF3 protein, human; D014157:Transcription Factors; D000071163:Trefoil Factor-1; D000071164:Trefoil Factor-2; D000071165:Trefoil Factor-3; D025521:Tumor Suppressor Proteins